title: Reversal of lead-induced toxicity due to the effect of antioxidants.
abstract: This study was designated to evaluate the protective effect of glutathione (GSH) and N-acetyl cysteine (NAC) in reducing the concentration of lead acetate in blood and soft tissues (liver, kidney, and brain) and their ability to restore altered hematopoietic, hepatic, renal, and other biochemical variables that are indicative of tissue oxidative stress in male rats. Male Wistar rats (150 ± 10 g) were randomly divided into 6 groups. Group 1 served as control. Group 2 served as experimental control was administered lead acetate (50 mg/kg intraperitoneally) for 3 days. Group 3 and 4 served as therapeutic controls. Animals in groups 5 and 6 received reduced GSH (1 mg/kg intraperitoneally) and NAC (50 mg/kg orally) for 3 days after the administration of lead acetate, as in group 2. The levels of hepatic and renal markers such as alanine aminotransferase, aspartate aminotransferase, triglycerides, cholesterol, urea, and uric acid were significantly increased (P ≤ 0.05) following administration of lead acetate. Administration of GSH and NAC provided significant protection to thiobarbituric acid reactive substances levels and reduced GSH content in tissues. On the other hand, significant recovery in lead-sensitive biochemical indices, like δ-aminolevulinic acid dehydratase, δ-aminolevulinic acid, and lead concentration in blood and soft tissues also were observed. It was concluded that NAC provided maximum protection compared with reduced GSH.
authors.affiliation: Reproductive Biology and Toxicology Laboratory, UNESCO Satellite Center of Trace Element Research, and School of Studies in Zoology, Jiwaji University, Gwalior (M.P.), India.
authors.forename: Samta
authors.initials: S
authors.lastname: Sharma
authors.forename: Sadhana
authors.initials: S
authors.lastname: Shrivastava
authors.forename: Sangeeta
authors.initials: S
authors.lastname: Shukla
mesh_terms: D000111:Acetylcysteine / Q000494:pharmacology; D000410:Alanine Transaminase / Q000378:metabolism; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D001921:Brain / Q000187:drug effects / Q000378:metabolism; D002784:Cholesterol / Q000378:metabolism; D005978:Glutathione / Q000494:pharmacology; D007274:Injections, Intraperitoneal; D007668:Kidney / Q000187:drug effects / Q000378:metabolism; D007854:Lead / Q000493:pharmacokinetics / Q000633:toxicity*; D007855:Lead Poisoning / Q000188:drug therapy*; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D008297:Male; D009942:Organometallic Compounds / Q000097:blood / Q000493:pharmacokinetics; D018384:Oxidative Stress / Q000187:drug effects; D000623:Porphobilinogen Synthase / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D014527:Uric Acid / Q000378:metabolism
chemical_list: D000975:Antioxidants; D009942:Organometallic Compounds; D017392:Thiobarbituric Acid Reactive Substances; D014527:Uric Acid; D007854:Lead; D002784:Cholesterol; D000410:Alanine Transaminase; D000623:Porphobilinogen Synthase; D005978:Glutathione; C008261:lead acetate; D000111:Acetylcysteine